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Resveratrol protects against oxidative stress by activating the Keap-1/Nrf2 antioxidant defense system in obese-asthmatic rats

机译:白藜芦醇通过激活肥胖性哮喘大鼠的Keap-1 / Nrf2抗氧化剂防御系统来防御氧化应激

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摘要

The aim of the present study was to investigate the potential mechanism underlying the anti-obesity-asthmatic effects of resveratrol (RSV) in a rat model of obese-asthma. Rat models of obesity and asthma were established using a high-fat diet and the administration of ovalbumin, respectively. Rats were divided into 7 different groups: A normal control, a normal obese, a normal asthma, a normal obese + asthma, a RSV obese, a RSV asthma and a RSV obese + asthma group. Body weight, Lee index, body fat and lung histopathological changes were evaluated. Serum lipid levels were evaluated using calorimetric methods. Levels of reactive oxygen species (ROS) were examined using enzyme-linked immunosorbent assays. Cellular antioxidant enzyme activities were measured using commercial kits. Levels of kelch-like ECH associated protein 1 (Keap-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) was examined using western blot analysis. The results indicated that obese and asthma rat models were successfully established. It was also demonstrated that RSV decreased fasting blood glucose in obese, asthmatic and obese-asthmatic rats. RSV altered serum lipid levels; it significantly increased high density lipoprotein cholesterol levels and significantly decreased serum triglyceride, serum total cholesterol and very low density lipoprotein levels, compared with untreated obese, asthmatic and obese-asthmatic rats (P<0.05). ROS levels were significantly decreased in the RSV treatment group compared with obese, asthmatic and obese-asthmatic rats (P<0.05). RSV treatment significantly increased catalase, glutathione, glutathione peroxidase and total superoxide dismutase levels compared with untreated obese, asthmatic and obese-asthmatic rats (P<0.05). Furthermore, RSV treatment significantly downregulated Keap-1 and upregulated Nrf2 levels in the heart, lung and kidney tissues of rats compared with untreated controls. Therefore, the results demonstrate that RSV protects against oxidative stress by activating the Keap-1/Nrf2 antioxidant defense system in obese-asthmatic rat models.
机译:本研究的目的是研究在肥胖哮喘大鼠模型中白藜芦醇(RSV)的抗肥胖-哮喘哮喘作用的潜在机制。使用高脂饮食和卵清蛋白分别建立肥胖和哮喘的大鼠模型。将大鼠分为7个不同的组:正常对照组,正常肥胖,正常哮喘,正常肥胖+哮喘,RSV肥胖,RSV哮喘和RSV肥胖+哮喘组。评估体重,李指数,体脂和肺组织病理学变化。使用量热法评估血清脂质水平。使用酶联免疫吸附法检测活性氧(ROS)的水平。使用商业试剂盒测量细胞抗氧化酶活性。使用蛋白质印迹分析检查了海藻样ECH相关蛋白1(Keap-1)和核因子类红细胞2相关因子2(Nrf2)的水平。结果表明成功建立了肥胖和哮喘大鼠模型。还证实了RSV降低了肥胖,哮喘和肥胖哮喘大鼠的空腹血糖。 RSV改变了血脂水平;与未治疗的肥胖,哮喘和肥胖哮喘的大鼠相比,它显着增加了高密度脂蛋白胆固醇的水平,并显着降低了血清甘油三酯,血清总胆固醇和极低密度脂蛋白的水平(P <0.05)。与肥胖,哮喘和肥胖哮喘的大鼠相比,RSV治疗组的ROS水平显着降低(P <0.05)。与未治疗的肥胖,哮喘和肥胖哮喘的大鼠相比,RSV治疗显着增加了过氧化氢酶,谷胱甘肽,谷胱甘肽过氧化物酶和总超氧化物歧化酶水平(P <0.05)。此外,与未治疗的对照组相比,RSV治疗可显着下调大鼠心脏,肺和肾脏组织中的Keap-1并上调Nrf2水平。因此,结果表明,RSV通过激活肥胖哮喘大鼠模型中的Keap-1 / Nrf2抗氧化剂防御系统来防御氧化应激。

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